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, René Rizzoli Service of Bone Diseases, WHO Collaborating Center for Osteoporosis Prevention, Department of Rehabilitation and Geriatrics, University Hospital, Geneva, Switzerland Search for other works by this author on: Oxford Academic Jean‐Philippe Bonjour Service of Bone Diseases, WHO Collaborating Center for Osteoporosis Prevention, Department of Rehabilitation and Geriatrics, University Hospital, Geneva, Switzerland Search for other works by this author on: Oxford Academic
Journal of Bone and Mineral Research, Volume 19, Issue 4, 1 April 2004, Pages 527–531, https://doi.org/10.1359/JBMR.040204
Published:
02 December 2009
Article history
Received:
02 January 2004
Revision received:
04 February 2004
Accepted:
05 February 2004
Published:
02 December 2009
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René Rizzoli, Jean‐Philippe Bonjour, Dietary Protein and Bone Health, Journal of Bone and Mineral Research, Volume 19, Issue 4, 1 April 2004, Pages 527–531, https://doi.org/10.1359/JBMR.040204
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INTRODUCTION
UNDERNUTRITION, PARTICULARLY PROTEIN malnutrition, is frequent in the elderly with osteoporotic hip fracture. On the other hand, high protein intake has been claimed to be harmful for bone health. This editorial addresses the issue of dietary protein in the pathogenesis and/or management of osteoporosis.
DIETARY PROTEIN AND BONE METABOLISM
High protein intake has been claimed to be a risk factor for osteoporosis. The proposed underlying mechanism implies that increasing protein intake increases acid production and renal acid excretion, because of protons released during the oxidation of sulfur‐containing amino acids such as methionine, cysteine, and cystine. Because urinary calcium excretion directly varies with acid excretion, urinary calcium is positively correlated with protein intake.(1) These associations would thus suggest that high protein intake will in turn induce a negative calcium balance and consequently would favor bone loss.(2) Furthermore, nutrition‐generated acid load would lead to an increased bone dissolution in healthy individuals, analogous to the classical physico‐chemical in vitro observation indicating that lowering pH favors the dissolution of calcium phosphate crystals, including those of hydroxyapatite. However, further studies indicate that a reduction in dietary protein may lead to a decline in calcium absorption and to secondary hyperparathyroidism.(3, 4) A low (0.7 g/kg body weight), but not a high (2.1 g/kg), protein intake was associated with an increase in biochemical markers of bone turnover compared with a diet containing 1.0 g/kg of protein.(5) High meat diets (1.6 g/kg body weight of protein) compared with 0.9 g/kg for 8 weeks did not affect calcium retention or indices of bone metabolism.(6) The question as to whether the source of proteins, animal versus vegetal, would differently affect calcium metabolism has been the object of more emotional belief than serious scientific demonstration.(7) This belief lies on the hypothesis that animal proteins would generate more sulfuric acid from sulfur‐containing amino acids than a vegetarian diet. That animal protein in contrast to vegetal protein would be consistently detrimental for bone health is not supported by chemical and experimental evidence. Indeed, a vegetarian diet, with protein derived from grains and legumes, would deliver as many millimoles of sulfur per gram proteins as would a purely meat‐based diet.(7, 8) On the other hand, it is true that meats contain substances other than sulfur acid‐producing substances. However, the net release of proton buffers from bone mineral does not seem to significantly contribute to blood acid‐base equilibrium, even in response to a conspicuous proton load, unless renal function is severely impaired.(9) High protein intakes are not associated with significant changes in blood pH.(10) However, in favor of this endogenous acid production in bone metabolism, it seems that neutralization of this endogenous acid production with potassium bicarbonate is associated with positive calcium balance.(11) In a cross‐sectional survey, BMD was higher in subjects with diets rich in fruits and vegetables, presumably rich in alkali.(8, 12) This issue is further complicated by the fact that the vegetable intake‐induced decrease in bone resorption(13) has been shown to be independent of acid‐base changes(14) and that potassium, but not sodium bicarbonate (i.e., the same anion) or citrate, administration reduces urinary calcium excretion.(1, 15) Finally, if high protein intake was really harmful for the skeleton, some consistent inverse relationship should be detected between BMD and dietary protein.
Issue Section:
Editorial
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